Lumbar spinal stenosis by amyloid thickening of the ligamentum flavum

Symptomatic lumbar canal stenosis without bony stenosis has previously been described. We describe the pathological modifications of ligamentum flavum among such operated patients. Ten patients were prospectively included in this study. Their mean age was 74, ranges: from 52-90 Clinical manifestation was a radicular claudication (sciatic or crural). Neuroradiology confirmed in all cases the ligamentum f lavum thickeness as the main cause of the symptomatology. This feature was also confirmed operatively and complete resection of the ligamentum flavum was performed. Resolution of the radicular pain was obtained in all cases a t last follow-up. Pathological examination of the ligamentum flavum display ed characteristic features of degenerative modifications and elastic fibers fragmentation caused by numerous amorphous deposits. The deposits were stu died using red Congo staining, polarized light and immunostaining methods. Such technique showed evidence of amyloid origin of the deposits. Immunodet ection was positive for the P component in the amyloid deposits and for bet a-2-microglobulin in one case (chronic renal failure and hemodialysis). The deposits did not express antitransthy retin antibodies. In parallel, contr ol ligamentum flavum were obtained from 10 operated patients affected by bo ny lumbar stenosis. Moderate degenerative features were observed but small amounts of amyloid deposits were found in only 3 of those cases, without th ickening of the ligamentous structure. This study correlates the presence of thickened ligamentum flavum caused by amyloid deposition, with symptomatic non-osseous lumbar canal stenosis. As sociation with degenerative modifications of the spine in the studied cases is suggestive of a microtraumatic origin.